**18. Carotid endarterectomy and stenting in specific situations**

#### **18.1. Restenosis after carotid stenting**

The restenosis rate after carotid stenting is remarkably low at 2.3-10% compared to other endovascular interventions. Although self-expanding carotid stents generate considerable neointimal hyperplasia, the process is balanced by marked late stent enlargement. Small stent dimensions immediately post-procedure were associated with a higher risk of restenosis.[32] In the 2003 global carotid stent registry, restenosis rates have been 2.7%, 2.6%, and 2.4% at 1, 2, and 3 years, respectively.[9] A retrospective, single-center review was conducted of 399 carotid stent procedures in 363 patients over 9 years, with a mean follow-up of 24 months (range 6-99 months). Overall, restenosis occurred in 15 patients (3.8%). However, the restenosis occurred in 7 of 35 (20%) patients who had previous neck radiation, 6 of 57 (10.5%) patients who had previous CEA, and 2 of 9 (22%) patients who previously had both CEA and neck radiation. The only analyzed variables that were significantly associated with an increased risk of restenosis were previous CEA (OR 4.28, P = 0.008) or XRT (OR 11.3, P <or=<or= 0.0001).[33] In another study, among 215 CAS procedures that had clinical and serial carotid duplex ultrasound investigations, restenosis was detected in 6.1% of patients. Contralateral carotid occlusion (OR 10.11, 95% CI 2.06-49.63, p = 0.004), carotid endarterectomy (CEA) restenosis (OR 8.87, 95% CI 1.68-46.84, p = 0.010) and postprocedural carotid duplex ultrasound with a PSV >/=120 cm/s (OR 6.33, 95% CI 1.27-31.44, p = 0.024) were independent predictors of stent restenosis.[34] Most restenoses occur within 6 to 12 months after the intervention. Usually they are located either in the mid or at the distal end of the stent. Restenoses are often overestimated by ultrasound compared to angiography. Most of restenoses can be treated by balloon angioplasty. Drug-eluting balloons can be a promising modality[35] and only rarely, stent removal and eversion endarterectomy will be required.[36]

#### **18.2. Restenosis after carotid endarterectomy**

There was no differential treatment effect with regard to the primary end point according to symptomatic status (P = 0.84) or sex (P = 0.34). The 4-year rate of stroke or death was 6.4% with stenting and 4.7% with endarterectomy (hazard ratio, 1.50; P = 0.03); the rates among symp‐ tomatic patients were 8.0% and 6.4% (hazard ratio, 1.37; P = 0.14), and the rates among asymptomatic patients were 4.5% and 2.7% (hazard ratio, 1.86; P = 0.07), respectively. Peri‐ procedural rates of individual components of the end points differed between the stenting group and the endarterectomy group: for death (0.7% vs. 0.3%, P = 0.18), for stroke (4.1% vs. 2.3%, P = 0.01), and for myocardial infarction (1.1% vs. 2.3%, P = 0.03). After this period, the incidences of ipsilateral stroke with stenting and with endarterectomy were similarly low

The results of the CREST were "satisfying" for both surgeons and interventionists. Surgeons were glad to prove that CEA resulted in lower stroke rates in the short term and the long term. Interventionists were reassured that the primary end-point was similar in the two methods. Restenosis and occlusion were infrequent and rates were similar up to 2 years after carotid endarterectomy and carotid artery stenting. Subsets of patients could benefit from early and

CAS was associated with better health-related quality of life HRQOL during the early recovery period as compared with CEA-particularly with regard to physical limitations and pain-but these differences diminish over time and are not evident after 1 year. Although CAS and CEA are associated with similar overall quality of life at 1 year, event-specific analyses confirm that

The MI rates were slightly lower after CAS (1.3% vs. 2.6%; P =.24). In performing CAS, vascular surgeons had outcomes for the periprocedural primary end point comparable to the outcomes of all interventionists (HR, 0.99; 95% CI, 0.50-2.00) after adjusting for age, sex, and symptomatic status. Vascular surgeons also had similar results after CEA for the periprocedural primary

The restenosis rate after carotid stenting is remarkably low at 2.3-10% compared to other endovascular interventions. Although self-expanding carotid stents generate considerable neointimal hyperplasia, the process is balanced by marked late stent enlargement. Small stent dimensions immediately post-procedure were associated with a higher risk of restenosis.[32] In the 2003 global carotid stent registry, restenosis rates have been 2.7%, 2.6%, and 2.4% at 1, 2, and 3 years, respectively.[9] A retrospective, single-center review was conducted of 399 carotid stent procedures in 363 patients over 9 years, with a mean follow-up of 24 months (range 6-99 months). Overall, restenosis occurred in 15 patients (3.8%). However, the restenosis occurred in 7 of 35 (20%) patients who had previous neck radiation, 6 of 57 (10.5%) patients who had previous CEA, and 2 of 9 (22%) patients who previously had both CEA and neck

stroke has a greater and more sustained impact on HRQOL than MI.[30]

end point compared with other surgeons (HR, 0.73; 95% CI, 0.42-1.27).[31]

**18. Carotid endarterectomy and stenting in specific situations**

(2.0% and 2.4%, respectively; P = 0.85).[28]

116 Carotid Artery Disease - From Bench to Bedside and Beyond

frequent monitoring after revascularization.[29]

**18.1. Restenosis after carotid stenting**

The incidence ranges from 1.2% to 23.9% depending on the operative technique. The highest rates of restenosis, 21.4%, after CEA came with direct suture and the lowest rate 3.9% were after patch angioplasty only Long-term risk of recurrence is about 1% per year. The risk is highest in the first few years after CEA and is very low later.[37]. Most of restenoses are asymptomatic and only 1.2-3.6% require re-intervention.[38]

The type of operative technique for reoperations depends on the cause of the recurrent disease. Myointimal hyperplasia has a smooth luminal surface and appears to be associated with a low potential for embolization therefore simple patching may be all that is necessary. By contrast, the soft nature of the plaque in recurrent atherosclerosis, which appears later, has a greater potential for embolization therefore repeat CEA with carotid patch angioplasty is preferable. AbuRahma et al showed the 30-day perioperative stroke and transient ischemic attack rates for reoperation and primary CEA were 4.8% versus 0.8% (P=0.015) and 4% versus 1.1%, respectively. There was an increase in the number of transient cranial nerve injuries in the reoperation group compared with the primary CEA group (15.3% versus 4.9%).[39]

CAS for restenosis after CEA has a complication rate lower than primary CAS. The time interval between CEA and CAS did not influence micro embolic load.[40] Statistical analysis demonstrated that post-CEA restenosis was the most important predictive factor for the development of in-stent restenosis after CAS. This review of our 10-year experience confirms that patients who develop restenosis after CEA are also prone to developing in-stent restenosis after CAS.[41]

#### **18.3. Carotid stenosis in patients requiring bypass cardiac surgery**

Patients who have concomitant severe carotid and coronary artery disease pose a serious dilemma. Stroke remains a major non-cardiac complication after CABG and myocardial infarction is the major non-neurological cause of early and late morbidity after CEA. The risk of stroke after CABG ranges from 0.7-5.2%[42]

Hemodynamically significant carotid stenoses are associated with 30% of early post-CABG strokes. The perioperative stroke risk is <2% when carotid stenoses are <50%, 10% when stenoses are 50% to 80%, 11% to 18.8% in patients with stenoses >80%. The risk shoots to 20% with untreated, bilateral, high-grade stenoses or an occluded carotid artery and contralateral high-grade stenosis.[43]

**3.** Ignoring the carotid disease initially and addressing it weeks to months later after the CABG procedure may be another approach. This idea is supported by a retrospective review of 94 patients with asymptomatic high-grade carotid stenosis undergoing CABG. There was one perioperative stroke and no deaths in this group of patients. These data combined with findings of Naylor et al that prophylactic CEA could barely prevent < 40% of post-CABG strokes [43] would support this approach in asymptomatic carotid stenoses. In the absence of clear guidelines, the decision is better individualized dealing with the more symptomatic vascular bed first. The simultaneous performance of CABG and CEA carries a high risk but is warranted in patients with recent symptoms of both severe

Update on Carotid Revascularization: Evidence from Large Clinical Trials

http://dx.doi.org/10.5772/57153

119

Carotid stenting can be an alternative in endarterectomy in this subset of patients.[45, 46] A recent Comparison of Early and Late Outcomes with Three Approaches to Carotid Revascu‐ larization and Open Heart Surgery showed that Staged CAS-OHS and combined CEA-OHS are associated with similar risk of death, stroke or MI in the short term, with both being better than staged CEA-OHS. However, the outcomes are significantly in favor of staged CAS-OHS

Patients with contralateral carotid occlusion have higher surgical risk for CEA due to multiple reasons; reduced collateral circulation during carotid clamping, cerebral hemorrhage secon‐ dary to hyperperfusion syndrome, and the overall advanced status of the vascular disease. Surgical mortality was extremely high in patients with a contralateral carotid occlusion and only 34% of the surgically treated patients were alive at 66 months in contrast to 63% of medically treated patients.(88) Results from the NASCET study demonstrated that medically treated patients with a contralateral occluded carotid were more than twice as likely to have a stroke compared to patients with a patent contralateral artery. However, when compared with medically treated patients, the overall risk of stroke contralateral to an occluded carotid artery was significantly reduced in the surgical patients. The risk of stroke in medically treated patients was 69% at 2 years versus 22% in patients treated surgically. (2) Thus, CEA with contralateral occlusion is a risky procedure but its risk may be justified considering the natural

The influence of the industry is strong, where all the industry-sponsored registries had lower rates of complications compared to randomized trials. The levels of expertise of operators vary significantly among trials as well as the obligatory use of protection devices. The percentage of symptomatic and asymptomatic patients also varies rendering interpretation of results and

coronary disease (unstable angina) and severe carotid stenosis.

**20. CEA in the presence of contralateral occlusion**

after the first year.[47]

history of the disease.

**21. CEA vs. CAS in the real world**

**21.1. The limitations of published trials comparing CEA and CAS**

The majority of strokes happen after the first 24 hours post CABG. This suggests that majority of strokes cannot be simply be ascribed to an adverse intra-operative event (low flow, hypo‐ tension and carotid embolism). The overall case fatality following post-CABG stroke as 23.1%. [43]In real life, it is not possible to state how often carotid stenosis of any degree of severity contributes to the incidence of ischemic stroke after CABG. Naylor et al concluded that primary carotid thromboembolic disease alone was not responsible for up to 59% of post CABG strokes. A significant proportion of post-operative strokes was in the vertebro-basilar territory or located contralateral to the severely stenosed carotid or ipsilateral to an insignificant stenosis. Aortic arch atherosclerosis embolization may be an important cause of stroke in the majority of cases.[43]
